A new study conducted by scientists at the Washington University School of Medicine indicates that sleep problems in youth and young adulthood could be an early indicator of Alzheimer’s disease.

The study used mice genetically altered to develop Alzheimer’s plaques in their brains as they aged. The researchers found that those mice that developed brain plaques also exhibited disrupted sleep-wake cycles.

“When the animals are young, there is no pathology in the brain, but as they get older they develop Alzheimer’s pathology in the brain, and at the same time they developed sleep-wake problems,” said senior author David Holtzman, M.D., the Andrew B. and Gretchen P. Jones professor and head of Washington University’s Department of Medicine. “Mainly, they would be awake much more of the time when they should be sleeping.”

Another indicator of the disease, researchers believe, could be a protein in the brain called amyloid beta. In healthy mice, scientists found that the amyloid beta level in cerebrospinal fluid fluctuated, increasing during waking hours and decreasing during sleep. This same fluctuation in the amyloid beta was seen in humans in a study by co-author Randall Bateman, M.D., a Charles F. and Joanne Knight distinguished professor of neurology at Washington University.

The new research suggests that the normal fluctuation of amyloid beta changes in both mice and humans when brain plaques begin to develop. According to Holtzman, these changes can occur up to 15 years before the usual cognitive symptoms associated with Alzheimer’s become evident in patients.

Researchers vaccinated another group of mice that had the same genetic mutations as the first group of mice to confirm the relationship between the protein amyloid beta and sleep. With time, however, the second group did not develop the same brain plaques, maintaining regular sleep-wake cycles and amyloid beta fluctuation in the brain.

Jee Hoon Roh, M.D. and Ph.D., a neurologist and postdoctoral fellow in Holtzman’s laboratory who led the research, said that the relationship between the amyloid beta fluctuation and sleep is reciprocal.

“Changes in the sleep pattern, in both humans and animals, show that the amount of sleep can increase amyloid beta and other pathogens in the brain,” Roh said. “Other studies show that the protein and other pathogens can disrupt sleep patterns. The relationship goes in both directions.”

The research also suggests that prolonged and chronic sleep deprivation in youth may influence one’s propensity to develop Alzheimer’s.

“Given from these types of studies in animals, chronic sleep deprivation over a long period of time—years—could potentially put us at risk for Alzheimer’s,” Holtzman said. The exact period of time that could put one at risk, however, is still unknown.

Another potential benefit of sleep-focused Alzheimer’s studies is the potential for earlier detection of the disease. According to Roh, late detection is one of the biggest obstacles to effective treatment of the disease.

Researchers are now looking into whether sleep problems have also been tracked in patients who have early symptoms of Alzheimer’s, such as plaque in the brain, but have not developed cognitive problems.

Bateman believes that Alzheimer’s research focusing on sleeping patterns could be crucial to better understanding and treating the disease.

“It is important to know the relationship between sleep and Alzheimer’s disease [in order] to see if one causes a risk because then we can do something about it by changing sleep habits and sleep hygiene,” Bateman said.